Small bowel intussusception caused by lymphomatous polyposis in a patient with AIDS.
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Acute Disease↗
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A Drosophila homolog of the tumor suppressor gene adenomatous polyposis coli down-regulates beta-catenin but its zygotic expression is not essential for the regulation of Armadillo.
Mutations in the adenomatous polyposis coli gene (which encodes a protein called APC) are associated with the formation of intestinal polyps and colon cancers. To facilitate the functional study of APC we have isolated its Drosophila homolog (D-APC) by screening an expression library with an antibody against human APC. The isolated cDNA encodes a predicted 2416-amino acid protein containing significant homology to multiple domains of mammalian APCs. D-APC has seven complete armadillo repeats with 60% identity to its human homolog, one beta-catenin binding site, and up to 7 copies of a 20-amino acid repeat with the average of 50% identity to human APC at amino acid level. D-APC, like its human counterpart, also contains a basic domain. Expression of the domain of D-APC homologous to the region required for beta-catenin down-regulation resulted in down-regulation of intracellular beta-catenin in a mammalian cell line. This same region bound to the Armadillo (Arm) protein, in vitro, the Drosophila homolog of beta-catenin. D-APC RNA and protein expression is very low, if detectable at all, during stages when Arm protein accumulates in a striped pattern in the epidermis of the Drosophila embryos. Removing zygotic D-APC expression did not alter Arm protein distribution, and the final cuticle pattern was not affected significantly. As observed in the rodent, high levels of D-APC expression have been detected in the central nervous system, suggesting a role for D-APC in central nervous system formation.
Adenomatous Polyposis Coli Protein↗
Accelerated growth of intestinal tumours after radiation exposure in Mlh1-knockout mice: evaluation of the late effect of radiation on a mouse model of HNPCC.
Mlh1-knockout mice have been developed as a useful model of hereditary non-polyposis colorectal cancer (HNPCC). In this study, we analyzed the pathology of gastrointestinal tumours (GIT) in these mice in detail and examined the possible effects of ionizing radiation on the induction of intestinal tumours to evaluate the late response to radiotherapy in HNPCC. Mlh1-/- mice spontaneously developed GIT and thymic lymphomas by 48 weeks. GIT included not only well differentiated adenocarcinomas but also poorly differentiated and mucinous adenocarcinomas, suggesting that this mouse is a good model for HNPCC. In contrast to colon cancers from HNPCC patients, however, carcinomas of Mlh1-/- mice expressed p53 and showed a lack of transforming growth factor (TGF)-betaRII mutation, which resulted in the expression of TGF-betaRII protein. Irradiation of 10-week-old Mlh1-/- mice accelerated GIT development but had little effect at 2 weeks. Mlh1+/- and Mlh1+/+ mice were not susceptible to spontaneous or radiation-induced thymic lymphomas and GIT until 72 weeks after birth. The development and pathology of GIT in Mlh1-/- mice suggest that this mouse is a good model for HNPCC, although tumour-related responsible genes might be different from HNPCC. As X-ray exposure promoted carcinogenesis of GIT in adult Mlh1-/- mice, an increased risk of secondary cancers after radiotherapy for HNPCC patients should be taken into consideration.
Adaptor Proteins, Signal Transducing↗
Biomechanical stabilization of the nipple valve in continent ileostomy.
Despite stapler stabilization, sliding complication of nipple valve function occur in 19 per cent of continent ileostomies. Because the tendency of the ileum to desuscept is triggered by traction forces on the mesentery of the nipple during filling of the reservoir, a technique was developed to neutralize this biomechanical strain. In addition, to obtain fibrous healing between the muscular layers, the mucosa of contacting intestinal walls was removed by selective ultrasonic fragmentation. The valves of 18 consecutive patients were operated on with this technique. In six of these, a sliding valve was restabilized in a median time of 1.2 (range 0.4-2.9) years after conventional construction of the pouch. All are functioning well after a median of 4.6 (range 3.0-6.0) years. Between 1.8 and 4.8 years after operation a healed area between the musculature of the nipple and pouch of 4.5-7.2 cm2 was shown by endosonography. This procedure may provide long-term prevention of sliding complications in continent ileostomies.
Adenomatous Polyposis Coli↗
[Cell proliferation of the intestinal mucosa in patients with familial adenomatosis coli. Autoradiography study].
In connection with routine endoscopic examinations of 31 patients with familial adenomatosis coli and 28 healthy kindreds of patients with familial adenomatosis coli we investigated by autoradiography the in vitro incorporation of 3H-thymidine into bioptic mucosal particles from colon and adenomas. Within the 5-year follow-up period there was found a significantly increased labelling index of polyps and the surrounding mucosa in patients with polyposis independing on the time elapsed after operation. In 12 of 28 kindreds the histological normal colonic mucosa showed an increased labelling index too. The prognostic value of these results must be proved by further controls.
Adenomatous Polyposis Coli↗
Pectin and methyl cellulose do not affect intestinal function in patients after ileal pouch-anal anastomosis.
OBJECTIVES: Although ileal pouch-anal anastomosis is the procedure of choice for most patients with ulcerative colitis or familial adenomatous polyposis, most patients have problems with stool frequency and/or consistency. Although most clinicians recommend fiber supplementation for these patients, we could find no studies that prove the efficacy of this practice. The first purpose of this study was to document the effect of fiber supplementation on intestinal function in patients after ileal pouch-anal anastomosis. Because pectin, a soluble fiber supplement, has been reported to slow gastric and intestinal transit, we also hypothesized that pectin would be a superior fiber supplement in these patients. The second purpose, therefore, was to determine whether the effects of pectin on intestinal transit would result in decreased stool frequency in patients with an ileal pouch. METHODS: Thirteen patients who had undergone ileal pouch-anal anastomosis for ulcerative colitis were entered into a 9-wk crossover study. The protocol consisted of three 2-wk study periods, each of which was preceded by a 1-wk washout period. During the three study periods patients supplemented their diets, in random order, with Citrucel, 1 tablespoon twice daily; pectin, 1 tablespoon twice daily; or no supplement. Patients maintained detailed dietary and bowel function diaries. RESULTS: The effects (mean +/- SE) of Citrucel and pectin supplementation are summarized in Table 1. There was no significant effect of either supplement on stool frequency, pouch function, bloating, or stool consistency. In addition, there were no differences in continence. CONCLUSIONS: We found no evidence to support the common practice of fiber supplementation in patients with an ileal pouch. Furthermore, this study did not find that stool frequency decreased during supplementation with pectin. We conclude that there is little role for fiber supplementation in patients with an ileal pouch.
Adult↗
A germline mutation at the extreme 3' end of the APC gene results in a severe desmoid phenotype and is associated with overexpression of beta-catenin in the desmoid tumor.
Desmoid tumors arise sporadically or as part of the extraintestinal manifestations of familial adenomatous polyposis (FAP). In FAP, two distinct clinical presentations of the desmoid phenotype are seen: 1) one or a few desmoid tumors present predominantly in the abdominal wall or the abdomen; 2) a florid proliferation of tumors early in life, mostly near the axial skeleton or extremities. These different phenotypes have been associated with different sites of germline mutations in the adenomatous polyposis coli gene (APC gene). We present a large, French-Canadian kindred with a florid desmoid tumor phenotype caused by a germline mutation at codon 2643-2644 of the APC gene. The phenotype was characterized by the early onset of multiple tumors, arising near the axial skeleton and in proximal extremities. The penetrance of desmoid tumors was near 100% in this kindred. However, the expression of the disease was variable amongst the different affected relatives. Many gene carriers had cutaneous cysts. Polyposis of the colon was rarely observed in the affected individuals and we did not document upper gastro-intestinal polyps. The mutant APC allele did not express a stable truncated protein in vivo. Molecular analysis of the proband's tumor DNA revealed a somatic inactivating mutation of the wild-type allele. Immunohistochemistry on the tumor also demonstrated elevated levels of beta-catenin. The present study demonstrates that this extreme 3' APC mutation is associated with a severely penetrant desmoid phenotype and attenuated polyposis coli. It also suggests the involvement of the beta-catenin pathway in the development of desmoid tumors in FAP. The natural history of the disease is variable between individuals, and surgical interventions have to be timed appropriately due to the frequent recurrences.
3' Untranslated Regions↗
Restorative proctocolectomy in patients after previous intestinal or anal surgery.
Restorative proctocolectomy is now established as the procedure of choice in many patients with ulcerative colitis or familial polyposis coli as well as in some patients with multiple colorectal tumors, ischemia, trauma, or congenital abnormalities. Some patients, however, may have had previous pelvic, abdominal, or perineal surgery, which might be considered a contraindication to restorative proctocolectomy. In a consecutive series of 73 private patients undergoing restorative proctocolectomy under one surgeon, we have reviewed in detail 13 who had had previous "significant" abdominal, pelvic, or anal surgery. Eight patients had previously had surgery for fistula-in-ano or fissure-in-ano, two had had an anal sphincter repair, and three had undergone possibly compromising abdominal or pelvic surgery prior to restorative proctocolectomy. Twelve of the 13 made an uncomplicated recovery from restorative proctocolectomy, although one has since died from carcinomatosis. One patient died after closure of an ileostomy from a combination of enterocutaneous fistula, infection, bleeding, and a perforated duodenal ulcer. One patient developed sepsis, necessitating removal of the pouch, and is classified as a failure. Two of the remaining 11 have had minor long-term functional problems with nocturnal fecal incontinence, and one patient needs to catheterize the pouch to evacuate, but all three patients prefer a pouch to an ileostomy. Restorative proctocolectomy can be performed successfully even after previous pelvic, abdominal, or anal surgery with an acceptable complication rate when compared with pouch surgery in the uncompromised patient.
Anal Canal↗
Concomitant suppression of hyperlipidemia and intestinal polyp formation by increasing lipoprotein lipase activity in Apc-deficient mice.
Epidemiologically, a high-fat diet is associated with the risk of colon cancer. In addition, serum levels of triglycerides (TGs) and cholesterol have been demonstrated to be positively associated with colon carcinogenesis. We recently found that an age-dependent hyperlipidemic state (high serum TG levels) exists in Apc-deficient mice, an animal model for human familial adenomatous polyposis. The mRNA levels of lipoprotein lipase (LPL), which catalyzes TG hydrolysis, were shown to be downregulated in the liver and intestines of mice. Moreover, treatment with a peroxisome proliferator-activated receptor (PPAR) alpha agonist, bezafibrate, or a PPARgamma agonist, pioglitazone, suppressed both hyperlipidemia and intestinal polyp formation in the mice, with induction of LPL mRNA. PPARalpha and PPARgamma agonists are reported to exert anti-proliferative and pro-apoptotic effects in cancer cells. One compound that also increases LPL expression levels but does not possess PPAR agnostic activity is NO-1886. When given at 400 or 800 ppm in the diet, it suppresses both hyperlipidemia and intestinal polyp formation in Apc-deficient mice, with elevation of LPL mRNA. In conclusion, a decrease in serum lipid levels by increasing LPL activity may contribute to a reduction in intestinal polyp formation with Apc deficiency. PPARalpha and PPARgamma agonists, as well as NO-1886, could be useful as chemopreventive agents for colon cancer.
Age Factors↗
[Clinico-morphological aspects and treatment of polyps associated with cancer of the large intestine].
Among 218 patients with cancer of the large intestine, in 56 (25.7%), a tumor was associated with single, or multiple polyps. In morphological study, considerable dysplasia of glandular epithelium was revealed in 43.7%, and malignization--in 9.2% of accompanying polyps. Considering association of cancer with adenomas as one of the forms of large intestinal polyneoplasia, the authors recommend to perform in such patients typical radical operations in combination with endoscopic polypectomy, and extend the volume of resection only in polyp malignization with invasion of the tela submucosa, or diffuse polyposis.
Adenoma↗
[Polyps of the large intestine in children].
Polyps in the large intestine is a frequent disease in children. It is more often observed in boys than in girls aged 4 to 9. In most cases solitary polyps are observed (in 73,35%). Two-three polyps are met in 21,62% of cases. Polyposis is a rare disease--0,91%. The main symptom of polyps in children is hemorrhage from the anal orifice. The method of treatment is dependent on the amount, size, height of the situs and spread of the polyps. Dissection of polyps through the rectal speculum is used more frequently, rectoromanoscope is used in rarer cases (electroexcision and coagulation). Resection of the large intestine or colotomy and ablation of polyps can be successfully used in polyposis and high situs of polyps.
Adolescent↗
Mucosal proctectomy without reservoir.
Mucosal proctectomy with endorectal pull-through allows the removal of all colonic mucosa with preservation of continence. This operation was performed in 19 patients with familial polyposis coli and ulcerative colitis. A temporary loop ileostomy was used to defunctionalize the anastomosis. Intestinal continuity was restored in 17 of the 19 patients. Mean duration of follow-up was 29 months. All patients are continent, and the mean number of bowel movements per 24 hours is 6. Follow-up barium studies revealed a gradual dilatation of the terminal ileum within the rectal cuff which accounts for the decrease in the number of bowel movements. This operation eliminates the risk of carcinoma without compromising sphincter function.
Adolescent↗
The prevention of colorectal cancer by aspirin use.
Epidemiologic studies indicate strongly that aspirin use reduces the risk of colorectal cancer and adenoma by approximately 40 to 50%. Perhaps up to ten years of use may be required before a benefit is apparent in colorectal cancer. The chemo-preventive actions of aspirin and other non-steroidal anti-inflammatory agents (NSAIDs) in colorectal carcinogenesis are also supported by animal studies, and by intervention studies that demonstrate that the anti-inflammatory agent sulindac causes regression of adenomas in familial adenomatous polyposis. Despite this evidence, the clinical implications are not clear because of increased gastro-intestinal irritation and bleeding episodes related to chronic aspirin use. Emerging evidence suggests that the anti-tumor properties of NSAIDs may be related primarily to the inhibition of cyclooxygenase-2 (COX-2), one of the two isoenzymes of the COX enzyme family. If confirmed, a new generation of selective COX-2 inhibitors may retain some of the chemo-preventive properties of NSAIDs with fewer side-effects. Firm recommendations regarding the use of aspirin or other NSAIDs to prevent colorectal cancer must await further research. For now, the decision must lie with the patient, in consultation with his or her healthcare provider, after a careful weighing of all potential risks and benefits.
Animals↗
Mbd4 inactivation increases Cright-arrowT transition mutations and promotes gastrointestinal tumor formation.
Mbd4 (methyl-CpG binding domain 4) is a novel mammalian repair enzyme that has been implicated biochemically in the repair of mismatched G-T residues at methylated CpG sites. In addition, the human protein has been shown to interact with the DNA mismatch repair protein MLH1. To clarify the role of Mbd4 in DNA repair in vivo and to examine the impact of Mbd4 inactivation on gastrointestinal (GI) tumorigenesis, we introduced a null mutation into the murine Mbd4 gene by gene targeting. Heterozygous and homozygous Mbd4 mutant mice develop normally and do not show increased cancer susceptibility or reduced survival. Although Mbd4 inactivation did not increase microsatellite instability (MSI) in the mouse genome, it did result in a 2- to 3-fold increase in C-->T transition mutations at CpG sequences in splenocytes and epithelial cells of the small intestinal mucosa. The combination of Mbd4 deficiency with a germ line mutation in the adenomatous polyposis coli (Apc) gene increased the tumor number in the GI tract and accelerated tumor progression. The change in the GI cancer phenotype was associated with an increase in somatic C-->T mutations at CpG sites within the coding region of the wild-type Apc allele. These studies indicate that, although inactivation of Mbd4 does not by itself cause cancer predisposition in mice, it can alter the mutation spectrum in cancer cells and modify the cancer predisposition phenotype.
Animals↗
Role of the prostaglandin E receptor subtype EP1 in colon carcinogenesis.
Although the cyclooxygenase pathway of the arachidonic acid cascade has been suggested to play an important role in colon carcinogenesis, the molecular species of prostanoids and receptors involved have not been fully elucidated yet. We examined the development of aberrant crypt foci (ACFs), putative preneoplastic lesions of the colon, in two lines of knockout mice, each deficient in prostaglandin E receptors, EP1 and EP3, by treatment with the colon carcinogen, azoxymethane. Formation of ACFs was decreased only in the EP1-knockout mice to approximately 60% of the level in wild-type mice. Administration of 250, 500, or 1000 ppm of a novel selective EP1 antagonist, ONO-8711, in the diet to azoxymethane-treated C57BL/6J mice also resulted in a dose-dependent reduction of ACF formation. Moreover, when Min mice, having a nonsense mutation in the adenomatous polyposis coli gene, were given 500 ppm ONO-8711 in the diet, the number of intestinal polyps was significantly reduced to 57% of that in the basal diet group. These results strongly suggest that prostaglandin E2 contributes to colon carcinogenesis to some extent through its action at the EP1 receptor. Thus, EP1 antagonists may be good candidates as chemopreventive agents for colon cancer.
Animals↗
[Endoscopic colorectal polypectomy in children and adolescents].
Endoscopic polypectomy was performed in a total of 22 children and two adolescents aged 3 to 17 years. The most frequent symptom leading to examination was enterorrhagia. During 31 colposcopic examinations a total of 113 polyps was removed. From the histological aspect in all patients juvenile polyps were involved, only in one patient with familial polyposis a tubular adenoma was detected. No complications were observed. Endoscopic polypectomy from the large intestine and rectum in children is a safe and satisfactory method which replaces the standard surgical approach and is much more sparing for the child.
Adolescent↗
Mesenteric fibromatosis.
Mesenteric fibromatosis is commonly associated with Gardner's syndrome and familial polyposis. These lesions may have an insidious onset via compression of the small or large intestines, or may be noted for the first time during abdominal exploration for some other cause. Differential diagnosis may be difficult. We report a case of mesenteric fibromatosis with two recurrences, and two cases with no evidence of tumour recurrence.
Adult↗
Colorectal cancer: future population screening for early colorectal cancer.
Colorectal cancer (CRC) is one of the most frequent cancers in Western countries. The identification of individuals at risk and the early diagnosis of CRC are of critical importance since a large proportion can be prevented or cured by surgical removal before metastasis has occurred. With increasing understanding of the genetic basis of hereditary and sporadic (non-hereditary) CRC, it becomes feasible to detect genetic alterations by molecular techniques. Familial adenomatous polyposis (FAP), hereditary nonpolyposis colorectal cancer (HNPCC), as well as early stages of spontaneous CRC, can be diagnosed by molecular characterisation of the adenomatous polyposis coli (APC) gene, the RAS oncogene and other genes in DNA from peripheral blood, stool or intestinal biopsies. With a better understanding of the genetic events leading to malignant transformation, molecular population screening should allow us to identify individuals at risk as well as patients with an early and potentially curable CRC. At present, careful patient and family history, physical examination and testing for occult blood as well as colonoscopy are still the key elements for clinical patient management. Molecular diagnosis will hopefully soon complement these analyses and should result in a reduction of morbidity and mortality from CRC.
Adenomatous Polyposis Coli↗